Review Article

A Brain Centred View of Psychiatric Comorbidity in Tinnitus: From Otology to Hodology

Table 2

Tinnitus-related alterations “into” and “within” auditory pathways.

MethodsAlterations observedReferences

MRIReduced grey matter volume in bilateral auditory areas including the Heschl’s gyrus. [43]
Significant grey matter decrease in the right IC.[44]

fMRIAbnormal asymmetric IC activation in patients with lateralized tinnitus.[45]
The ratio of activation between right and left IC did not differ significantly between tinnitus and non-tinnitus patients or in a manner dependent on tinnitus laterality.[46]
Tinnitus-induced hyperactivity in the dorsal cochlear nucleus.[47]
Tinnitus-related hyperexcitability of auditory cortex.[48]
Significant signal change lateralized towards the side of perceived tinnitus in primary auditory cortex and IC in patients with right sided tinnitus and towards the medial geniculate body in patients with left sided tinnitus.[49]
Smaller medial partition of Heschl's gyrus gray matter volume.[50]

PETTinnitus-related elevated blood flow in auditory cortex.[51]
Focal metabolic activation in the predominant left auditory cortex.[52]
Significantly increased metabolic activity in the left primary auditory cortex; increased metabolic activity in temporal and parietal brain regions (in female tinnitus patients) and in frontal and occipital regions (in male tinnitus patients).[53]
Asymmetric activation of the auditory cortex, predominantly on the left side and independently from tinnitus laterality.[54]
Activation of left and right posterior inferior temporal gyrus as well as left and right posterior parahippocampal-hippocampal interface; overactivation of left in contrast to right Heschl’s gyrus independently from tinnitus laterality. [55]

MEGReduced alpha activity (8–12 Hz) and increased slow wave activity (delta and theta 1–6 Hz) and gamma activity (>30 Hz) in the temporal cortex.[56]

EEGAbnormal gamma band activity (>30 Hz) generated as a consequence of hyperpolarization of specific thalamic nuclei.[57]
Correlation between electroencephalographic gamma band activity in the contralateral auditory cortex and the presence of tinnitus.[58]
Discrete localised unilateral foci of high frequency activity in the gamma range (>40–80 Hz) over the auditory cortex.[59]
Reduced wave I (indicating reduced auditory-nerve activity) and elevated waves III and V amplitude (indicating hyperactivity of pathways originating from ventral cochlear nucleus) assessed via auditory brainstem responses.[60]
Increased neuronal activity in auditory pathways (long latency auditory evoked potentials).[61]
Cortical information processing dysfunction in chronic tinnitus patients associated with auditory stimuli.[62]

IC: Inferior Colliculus.